PMID: 

Brain Res. 1998 Oct 26 ;809(1):50-7. PMID: 9795129

Abstract Title: 

Evidence for the involvement of nitric oxide and nitric oxide synthase in the modulation of opioid-induced antinociception and the inhibitory effects of exposure to 60-Hz magnetic fields in the land snail.

Abstract: 

The attenuation of opioid peptide-mediated antinociception is a well-established effect of extremely low frequency (ELF) electromagnetic fields with alterations in calcium channel function and/or calcium ion flux and protein kinase C activity being implicated in the mediation of these effects. The present study was designed to examine the effects of nitric oxide (NO) and calcium ion/calmodulin-dependent nitric oxide synthase (NOS) on opioid-induced antinociception and their involvement in mediating the inhibitory effects of exposure to ELF magnetic fields. We observed that enkephalinase (SCH 34826)-induced, and likely enkephalin-mediated, antinociception in the land snail, Cepaea nemoralis, as measured by the enhanced latency of a foot withdrawal response to a thermal (40 degreesC) stimulus, was reduced by the NO releasing agent, S-nitro-N-acetylpenicillamide (SNP), and enhanced by the NO synthase inhibitor, NG-nitro-l-arginine methyl ester (l-NAME). Exposure of snails to an ELF magnetic field (15 min, 60 Hz, 141 microT peak) also reduced the enkephalinase-induced antinociception. The inhibitory effects of the 60-Hz magnetic field were significantly reduced by the NO synthase inhibitor, l-NAME, and significantly enhanced by the NO releasing agent, SNP, at dosages which by themselves had no evident effects on nociceptive sensitivity. These results suggest that: (1) NO and NO synthase have antagonistic effects on opioid-induced analgesia in the snail, Cepaea and (2) the inhibitory effects of ELF magnetic fields on opioid analgesia involve alteration in NO and NO synthase activity.

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PMID: 

Adv Clin Exp Med. 2015 Jan-Feb;24(1):31-5. PMID: 25923084

Abstract Title: 

The impact of electromagnetic radiation of different parameters on platelet oxygen metabolism – in vitro studies.

Abstract: 

BACKGROUND: Electromagnetic radiation emitted by a variety of devices, e.g. cell phones, computers and microwaves, interacts with the human body in many ways. Research studies carried out in the last few decades have not yet resolved the issue of the effect of this factor on the human body and many questions are left without an unequivocal answer. Various biological and health-related effects have not been fully recognized. Thus further studies in this area are justified.OBJECTIVES: A comparison of changes within catalase enzymatic activity and malondialdehyde concentration arising under the influence of the electromagnetic radiation emitted by car electronics, equipment used in physiotherapy and LCD monitors.MATERIAL AND METHODS: The suspension of human blood platelets at a concentration of 1× 109/0.001 dm 3, obtained from whole blood by manual apheresis, was the study material. Blood platelets were exposed to an electromagnetic field for 30 min in a laboratory stand designed for the reconstruction of the electromagnetic radiation generated by car electronics, physiotherapy equipment and LCD monitors. The changes in catalase activity and malondialdehyde concentration were investigated after the exposure and compared to the control values (unexposed material).RESULTS: An increase in catalase activity and malondialdehyde concentration was observed after 30 min exposure of platelets to EMF regardless of the radiation source. The most significant changes determining the degree of oxidative stress were observed after exposure to the EMF generated by car electronics.CONCLUSIONS: The low frequency electromagnetic fields generated by car electronics, physiotherapy equipment and LCD monitors may be a cause of oxidative stress in the human body and may lead to free radical diseases.

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Ever since news of the capabilities of cannabidiol (CBD) traveled from academia to the public, the plant extract has surged into mainstream use and wellness popularity.

After years of underground CBD sales and several clinical studies on its growing list of positive effects, the Agriculture Improvement Act of 2018, also known as the Farm Bill, was passed. This legalized the industrial cultivation and sale of hemp – consequently legalizing its derivatives, including CBD – and opened the floodgates for everything cannabidiol. Since then, the growth of the market has been so staggering that the industry is shaping up to be worth over $5 billion by the end of 2019, a 706% growth from 2018. Moreover, according to Brightfield Group’s 2019 report, the total U.S. CBD Market would reach $23.7 billion by 2023.

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Credits:

Source: https://www.forbes.com/

News Link: https://www.forbes.com/sites/joresablount/2019/10/01/new-study-reveals-nano-liposome-is-the-best-way-to-take-cbd/#11064ec9362c

The post New Study Reveals Nano-Liposome Is The Best Way To Take CBD appeared first on AlternativeWellness.

PMID: 

Eur J Pharmacol. 2019 Sep 15 ;859:172490. Epub 2019 Jun 21. PMID: 31229536

Abstract Title: 

Astragaloside IV alleviates doxorubicin induced cardiomyopathy by inhibiting NADPH oxidase derived oxidative stress.

Abstract: 

Doxorubicin (DOX) is a classic anti-tumor chemotherapeutic used to treat a wide range of tumors. One major downfall of DOX treatment is it can induce fatal cardiotoxicity. Astragaloside IV (AS-IV) is one of the primary active ingredients that can be isolated from the traditional Chinese herbal medicine, Astragalus membranaceus. This study uses both in vitro and in vivo tools to investigate whether AS-IV alleviates DOX induced cardiomyopathy. We found that AS-IV supplementation alleviates body weight loss, myocardial injury, apoptosis of cardiomyocytes, cardiac fibrosis and cardiac dysfunction in DOX-treated mice. Also, DOX-induced cardiomyocyte injury and apoptosis were effectively improved by AS-IV treatment in vitro. NADPH oxidase (NOX) plays an important role in the progress of the oxidative signal transduction and DOX-induced cardiomyopathy. In this study, we found that AS-IV treatment relieves DOX-induced NOX2 and NOX4 expression and oxidative stress in cardiomyocytes. In conclusion, AS-IV, an antioxidant, attenuates DOX-induced cardiomyopathy through the suppression of NOX2 and NOX4.

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PMID: 

Exp Anim. 2019 Jun 26. Epub 2019 Jun 26. PMID: 31243190

Abstract Title: 

Astragaloside IV reduces cardiomyocyte apoptosis in a murine model of coxsackievirus B3-induced viral myocarditis.

Abstract: 

Apoptosis plays a crucial role in regulating cardiomyopathy and injuries of coxsackievirus B3 (CVB3)-induced viral myocarditis (VM). It has been reported that Astragaloside IV (AST-IV) from Astragalus membranaceus could inhibit apoptosis under a variety of pathological conditions in vivo or in vitro. However, the functional roles of AST-IV in CVB3-induced VM still remain unknown. Here, we found that AST-IV significantly enhanced survival for CVB3-induced mice. AST-IV protected the mice against CVB3-induced virus myocarditis characterized by the increased body weight, decreased serum level of creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH), supressed expression of Ifn-γ, Il-6 in heart, enhanced systolic and diastolic function of left ventricle. At the pathological level, AST-IV ameliorated the mice against CVB3-induced myocardial damage and myocardial fibrosis. In vitro, the results from flow cytometry showed that AST-IV significantly suppressed CVB3-induced cardiomyocytes apoptosis, which also were verified in vivo. Moreover, an increased expression of pro-apoptotic genes including FAS, FASL, cleavedcaspase-8 and cleaved caspase-3 was found in CVB3-induced cardiomyocytes, while those was inhibited in cardiomyocytes treated with AST-IV. Taken together, the data suggest that AST-IV protected against CVB3-induced myocardial damage and fibrosis, which may partly attribute to supress activation ofFAS/FASL signaling pathway.

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PMID: 

Int J Mol Med. 2019 Sep ;44(3):847-856. Epub 2019 Jun 26. PMID: 31257467

Abstract Title: 

Astragaloside IV inhibits oxidized low‑density lipoprotein‑induced endothelial damage via upregulation of miR‑140‑3p.

Abstract: 

Oxidized low‑density lipoprotein (ox‑LDL)‑mediated endothelial cell injury has an important role in the vascular complications of type 2 diabetes. Astragaloside IV (ASV) is an active component of Radix Astragali, which has been demonstrated to exert protective effects against endothelial damage. The present study explored whether microRNAs (miRNAs) are involved in mediating the protective effects of ASV on ox‑LDL‑induced damage in human umbilical vein endothelial cells (HUVECs). RNA sequencing and reverse transcription‑quantitative PCR analyses revealed that ox‑LDL treatment significantly downregulated miR‑140‑3p expression in HUVECs. miR‑140‑3p overexpression promoted cell proliferation and inhibited apoptosis in ox‑LDL‑induced HUVECs. However, inhibition of miR‑140‑3p expression could reverse the effects of ASV on ox‑LDL‑induced HUVECs and reactivate ASV‑inhibited PI3K/Akt signaling in ox‑LDL‑induced HUVECs. In addition, Krüppel‑like factor 4 (KLF4) was identified as a target of miR‑140‑3p in ox‑LDL‑treated HUVECs. Subsequent experiments revealed that KLF4 overexpression partially counteracted the protective effects of miR‑140‑3p or ASVtreatment in ox‑LDL‑induced HUVECs. Taken together, the current findings demonstrated that the protective effects of ASV on HUVECs were dependent on miR‑140‑3p upregulation and subsequent inhibition of KLF4 expression, which in turn suppressed the PI3K/Akt signaling pathway. The present results shed light to the molecular mechanism by which ASV alleviated ox‑LDL‑induced endothelial cell damage.

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PMID: 

Oxid Med Cell Longev. 2019 ;2019:4625912. Epub 2019 Jun 11. PMID: 31285785

Abstract Title: 

Astragaloside IV Exerts a Myocardial Protective Effect against Cardiac Hypertrophy in Rats, Partially via Activating the Nrf2/HO-1 Signaling Pathway.

Abstract: 

Previous evidence suggested that astragaloside IV (ASIV) had a cardioprotective effect, but the potential mechanisms were undetermined. This study is aimed at validating the prevention of cardiac hypertrophy in chronic heart failure (CHF) rats and hypertrophy in H9c2 cardiomyocytes by ASIV and at exploring the potential mechanism involved. CHF rat models of abdominal aortic constriction (AAC) were used with the aim of determining the protective effect of ASIV in cardiac hypertrophy in the rats. We proved that ASIV could attenuate cardiac hypertrophy by improving left ventricular function and structure and showed that the expression of nuclear factor-erythroid 2-related factor 2 (Nrf2) and its downstream gene heme oxygenase-1 (HO-1) increased in the high-dose ASIV intervention group. To further investigate the specific mechanism of ASIV, we hypothesized that ASIV might prevent cardiac hypertrophy via activating the Nrf2/HO-1 signaling pathway. We established a cardiomyocyte hypertrophy model induced by angiotensin II (Ang II), which was then transfected with Nrf2 shRNA, to knock down the expression of the Nrf2 gene. We found that the protective effect of ASIV against Ang II-induced cardiomyocyte hypertrophy was abolished in the Nrf2 shRNA transfection group, ultimately aggravating cardiomyocyte hypertrophy induced by Ang II, and it is possible that oxidative stress may be involved in this process. Our results demonstrated that ASIV improved cardiac function and inhibited cardiac hypertrophy by upregulating Nrf2, and this effect was partially achieved by stimulating the Nrf2/HO-1 signaling pathway, suggesting that ASIV could have therapeutic potential for the treatment of cardiac hypertrophy and CHF.

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PMID: 

Immunopharmacol Immunotoxicol. 2019 Aug ;41(4):497-503. Epub 2019 Jul 11. PMID: 31293216

Abstract Title: 

Astragaloside inhibits IL-1β-induced inflammatory response in human osteoarthritis chondrocytes and ameliorates the progression of osteoarthritis in mice.

Abstract: 

Osteoarthritis (OA) is a chronic joint-degeneration disease and accounts for the most frequent arthritis in aging people. OA is characterized by the degeneration of articular cartilage, subchondral bone sclerosis and synovitis. Inflammation as an important role in OA progression, in that anti-inflammatory agents could effectively inhibit the development of OA with minimal side effects, therefore developing a nature anti-inflammatory compound will be a promising therapy for treating OA.We treated patient-derived chondrocytes and mouse models of OA with astragaloside, an effective component of, and measured its effect on pro-inflammatory cytokines and OA progression in mice., astragaloside induced a dose-dependent inhibition of IL-1β-induced the production of inflammatory factors, including interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), nitric oxide (NO), prostaglandin E2 (PGE2), expression of MMP 13 and ADAMTS-5, and the activation of NF-κB signaling., astragaloside ameliorate the degeneration of cartilage in mouse model of OA.Astragaloside potentially serve as a promising and effective therapeutic agent for treating OA patients.

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PMID: 

J Oral Pathol Med. 2019 Jul 18. Epub 2019 Jul 18. PMID: 31318999

Abstract Title: 

Astragaloside IV attenuates inflammatory injury and promotes odontoblastic differentiation in lipopolysaccharide-stimulated MDPC-23 cells and rat pulpitis.

Abstract: 

BACKGROUND: Astragaloside IV (AS-IV), a natural herbal compound from Astragalus membranaceus, has inhibitory effects on receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclastogenesis, and RANKL signal helps to regulate odontoblast differentiation. However, whether and how AS-IV affects odontoblastic differentiation remains unclear.METHODS: Lipopolysaccharide (LPS)-stimulated MDPC-23 cells and rat pulpitis were treated with AS-IV, cell viability, and LDH leakage was analyzed by CCK-8 assay and LDH Leakage assay. The production of TNF-α and IL-6 was determined by ELISA and qRT-PCR assay. The expression of alkaline phosphatase (ALP) was detected using an ALP assay kit, and the expression of dentin sialophos-phoprotein (DSPP), dentin matrix protein-1 (DMP1), basic fibroblast growth factor (FGF2), and phosphorylated extracellular signal-regulated kinase (p-ERK) was determined by western blot.RESULTS: AS-IV dose dependently increased in cell viability and decreased the overproduction of TNF-α and IL-6 in LPS-stimulated MDPC-23 cells. AS-IV also counteracted LPS-induced downregulation of ALP, DSPP, and DMP1 in MDPC-23 cells. Furthermore, AS-IV significantly decreased the expression of FGF2 and p-ERK in LPS-stimulated MDPC-23 cells. More important, the addition of FGF2 partly neutralized AS-IV-mediated inhibition of FGF2/ERK signaling, abolished AS-IV-induced reduction of TNF-α and IL-6, and counteracted AS-IV-induced upregulation of DSPP and DMP-1 in these cells. Meanwhile, AS-IV inhibited the excessive production of TNF-α and IL-6, suppressed the downregulation of DSPP and DMP1, and disturbed the up-regulation of FGF2 and p-ERK in the pulp tissues of rat pulpitis model.CONCLUSIONS: AS-IV exerted anti-inflammatory and pro-differentiation effects in LPS-stimulated MDPC-23 cells and rat pulpitis via inhibiting the FGF2/ERK signaling pathway.

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PMID: 

Oxid Med Cell Longev. 2019 ;2019:9137654. Epub 2019 Jun 24. PMID: 31341538

Abstract Title: 

Astragaloside IV Attenuates Myocardial Ischemia-Reperfusion Injury from Oxidative Stress by Regulating Succinate, Lysophospholipid Metabolism, and ROS Scavenging System.

Abstract: 

Astragaloside IV is one of the main active ingredients isolated from. Here we confirmed its protective effect against cardiac ischemia-reperfusion (I/R) injury and aimed to investigate the potential molecular mechanisms involved. Pretreatment ofandI/R-induced rat models by astragaloside IV significantly prevented the ratio of myocardium infarct size, systolic and diastolic dysfunction, and the production of creatine kinase and lactate dehydrogenase. Metabolic analyses showed that I/R injury caused a notable reduction of succinate and elevation of lysophospholipids, indicating excessive reactive oxygen species (ROS) generation driven by succinate's rapid reoxidization and glycerophospholipid degradation. Molecular validation mechanistically revealed that astragaloside IV stimulated nuclear factor (erythroid-derived 2)-like 2 (Nrf2) released from Kelch-like ECH-associated protein 1 (Keap1) and translocated to the nucleus to combine with musculoaponeurotic fibrosarcoma (Maf) to initiate the transcription of antioxidative gene heme oxygenase-1 (HO-1), which performed a wide range of ROS scavenging processes against pathological oxidative stress in the hearts. As expected, increasing succinate and decreasing lysophospholipid levels were observed in the astragaloside IV-pretreated group compared with the I/R model group. These results suggested that astragaloside IV ameliorated myocardial I/R injury by modulating succinate and lysophospholipid metabolism and scavenging ROS via the Nrf2 signal pathway.

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